Beschreibung
The state of health care is reflected by perinatal and neonatal morbidity and mortality as well as by the frequencies of long-term neurological and developmental disorders. Many factors, some without immediately recognizable significance to childbearing and many still unknown, undoubtedly contribute beneficially or adversely to the outcome of pregnancy. Knowledge concerning the impact of such factors on the fetus and surviving infant is critical. Confounding analyses of pregnancy outcome, especially these past 2 or 3 decades, are the effects of newly undertaken invasive or inactive therapeutic approaches coupled with the advent of high technology. Many innovations have been introduced without serious efforts to evaluate their impact prospectively and objectively. The consequences of therapeutic misadventures character ized the past; it seems they have been replaced to a degree by some of the complications of applied technology. Examples abound: after overuse of oxygen was recognized to cause retrolental fibroplasia, its restriction led to an increase in both neonatal death rates and neurologic damage in surviving infants. Administration of vitamin K to prevent neonatal hemorrhagic disease, particularly when given in what we now know as excessive dosage, occasionally resulted in kernicterus. Prophy lactic sulfonamide use had a similar end result. More recent is the observation of bronchopulmonary dysplasia as a complication of re spirator therapy for hyaline membrane disease. The decade of the eighties opened with the all-time highest rate of cesarean section in the United States.
Autorenporträt
Inhaltsangabe1 Antecedents of Childhood Obesity.- 1. Introduction.- 2. Criteria, Classification, and Prevalence.- 3. Interaction of Maternal Weight and the Neonate.- 4. Natural History.- 5. Adiposity and the Adipocyte.- 5.1. The Fat Cell Hypothesis.- 5.2. Test Methods.- 5.3. Critical Period for Determining Fat Cell Number Occurs Early in Life.- 5.4. Increased Adipose Cell Number Makes It Difficult or Impossible for the Individual to Lose Weight.- 5.5. Evidence for a Metabolic Defect Leading to Obesity.- 6. Intervention and Treatment.- References.- 2 The Embryology of Birth Defects: Malformations vs. Deformations vs. Disruptions.- 1. Introduction.- 2. Types of Malformations.- 2.1. Incomplete Morphogenesis.- 2.2. Aberrant Form.- 2.3. Hamartomata.- 2.4. Malformations Secondary to Lack of Fetal Movement.- 3. Deformations.- 3.1. Intrinsically Derived Prenatal Onset Deformations.- 3.2. Extrinsically Derived Prenatal Onset Deformations.- 4. Disruptions.- 4.1. Amniotic Bands.- 4.2. Interruption of Blood Supply.- 5. Conclusion.- References.- 3 Brain Metabolic and Pathologic Consequences of Asphyxia: Role Played by Serum Glucose Concentration.- 1. Fetal Asphyxia as Cause of Brain Injury.- 2. Traditional Concepts Concerning the Brain Metabolic Basis for Injury from Asphyxia.- 3. Brain Tolerance to Circulatory Arrest May Be Extended.- 4. Spurious Evidence That Administering Glucose Solutions Extends Brain Tolerance to Asphyxia.- 5. Evidence That Infusions of Glucose Solutions Reduce Rather Than Extend Brain Tolerance to Anoxia.- 6. Evidence That Infusions of Glucose Solutions Reduce Rather Than Extend Overall Animal Tolerance to Hypoxia.- 7. Hypothesis That Lactic Acid Accumulation beyond 17 to 20 µmoles/g Damages the Brain.- 8. Mechanisms through Which the Fall in Blood Pressure during Hypoxia Injures the Brain.- 9. Brain Biochemical Changes Produced by Hypoxia and Anoxia and Their Relation to Brain Injury.- 10. Mechanisms Which Operate during Hypoxia and during Anoxia to Increase Brain Tissue Lactic Acid Concentrations.- 11. Evidence that Infusions of Glucose Solutions during the Recovery Period Exacerbate Anoxic Brain Injury.- 12. Applicability to the Fetus and Newborn.- 13. Summary and Conclusions.- References.- 4 Bronchopulmonary Dysplasia Today.- 1. Introduction.- 1.1. Terminology and Definition of Bronchopulmonary Dysplasia.- 1.2. Perspective.- 2. Pathology of Bronchopulmonary Dysplasia.- 3. Incidence and Mortality of Bronchopulmonary Dysplasia.- 4. Etiology of Bronchopulmonary Dysplasia.- 4.1. General Considerations.- 4.2. Pulmonary Oxygen Toxicity.- 4.3. Assisted Ventilation.- 4.4. Underlying Diseases.- 4.5. Risk Factors for Bronchopulmonary Dysplasia.- 4.6. Mechanism of Lung Injury.- 5. Radiographic Appearance of Bronchopulmonary Dysplasia.- 5.1. Initial Description.- 5.2. Present Appearance of Bronchopulmonary Dysplasia.- 5.3. Atypical Appearances of Bronchopulmonary Dysplasia.- 5.4. Radiographic-Pathological Correlation in Bronchopulmonary Dysplasia.- 6. Radiographic Differential Diagnosis of Bronchopulmonary Dysplasia.- 6.1. Cautionary Remarks.- 6.2. Differential Diagnostic Considerations.- 7. Complications and Associations of Chronic Bronchopulmonary Dysplasia.- 7.1. Lower Respiratory Tract Infections.- 7.2. Cardiovascular Complications.- 7.3. Focal Atelectasis.- 7.4. Rib Fractures, Rickets, and Renal Calcifications.- 7.5. Cholelithiasis.- 8. Surveillance and Assessment of Bronchopulmonary Dysplasia.- 8.1. Acute Phases of Bronchopulmonary Dysplasia.- 8.2. Chronic Phases of Bronchopulmonary Dysplasia.- 9. Summary.- References.- 5 Neonatal Behavioral Effects of Anesthetic Exposure during Pregnancy.- 1. Introduction.- 2. Infant Neurobehavior-A Model Problem.- 3. Preconception and Chronic Exposure to Anesthetics.- 3.1. Incidental Exposure-Operating-Room Personnel.- 3.2. Incidental Exposure-Dental Personnel.- 3.3. Drug and Alcohol Addiction-Chronic.- 4. Gestational Exposure to Anesthetics.- 4.1. Animal Studies.- 4.2. Human Studies.- 5. Obstet
